茶葉萃取物(EGCG或TF-3-G)透過JNK訊息傳遞抑制HCT-116人類大腸癌細胞株之細胞週期進展

兒茶素(catechin)在近幾年癌症相關的研究中備受矚目，而兒茶素中以(-)-epigallocatchin-3-gallate(EGCG)的含量較為豐富，同時也能有效抑制癌症細胞的生長；至於全發酵的紅茶中，指出了茶黃質(theaflavins)也能有效抑制癌症細胞生長的效果。實驗調查了茶葉萃取物以及EGCG或TF-3-G對HCT-116 人類大腸癌細胞株之影響。結果顯示EGCG或TF-3-G透過G2/M停滯之影響，造成 HCT-116細胞生長的抑制作用。我們進一步觀察HCT-116細胞內的蛋白質表現， EGCG 或TF-3-G會活化JNK、p53和p21的表現量，但是會降低Cyclin A和 Cyclin B的表現量。當 HCT-116預先添加 JNK Inhibitor(SP600125)後，再加入EGCG或 TF-3-G進行反應，並會逆轉HCT-116細胞G2/M停滯的現象；當比較沒添加EGCG或TF-3-G蛋白質的表現時，p53、p21、cyclin A和cyclin B的蛋白質表現則沒有顯著的差異。實驗證實了EGCG或TF-3-G，會透過活化JNK訊息傳遞的機制，造成了HCT-116細胞生長的抑制，進一步改變cyclin A 和cyclin B 的蛋白質表現，並誘導細胞週期的停滯作用。

Catechins in cancer-related research have received great attention in recent years. The (-)-epigallocatechin-3-gallate (EGCG) are most abundant compound in extracted that effective inhibits the growth of cancer cells. Theaflavins extracted from completely fermented black tea are also inhibits the growth of cancer cells effectively. In this study, we use human colorectal cancer cell lines that were treated with tea extracts such as EGCG or TF-3-G, and their effects on the HCT116 cells were investigated. EGCG or TF-3-G inhibits the growth of HCT-116 cells through triggering the G2/M arrest in HCT-116. We further examined cellular-signaling protein and found that EGCG or TF3-G increase the activities of JNK and also p53 and p21 expression, but reduces Cyclin A and Cyclin B expression. HCT-116 cells pre-treated with JNK Inhibitor (SP600125) before adding EGCG or TF-3-G were examined and we found that EGCG or TF-3-G is able to reverse G2/M arrest in HCT-116, wherein p53, p21, cyclin A and cyclinB protein levels are not significantly changed comparison to cells without treated EGCG or TF-3-G. We found that EGCG or TF-3-G inhibits HCT-116 cells growth through mechanisms that influence on the activity of JNK signaling pathway, and future change cyclin A and Cyclin B expression levels to induce cell cycle arrest.